Genes, Antigens, Antibodies, and Basic Testing Flashcards by Natalie Hamill

Leucocyte Poor Red Cells

Used primarily for patients with repeated febrile non hemolytic (FNH) reactions or those that are chronically transfused

Usually due to the presence of cytokines released from white cells or alloimmunization to HLA or leukocyte antigens

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Differentiating A1 and A2

Based on reactivity differences with anti-A1, lectin from Dolichos biflorus, which agglutinates A1 but NOT A2 cells

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Anti-H Differentiation

Lectin from Ulex europaeus, which will agglutinate O cells (HH or Hh), but not Bombay cells (hh)

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Se gene

Two alleles, Se (secretors) and se

Allow expression of ABO and H (A, B, H, and Le^b) antigens in body fluids

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Combination of H and Le genes

H and Le^a will be on red cells, only Le^a only in saliva

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Combination of H, Se, and Le genes

H and Le^b on the red blood cells, H, Le^b, and Le^a in small amounts in body fluids

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Rh null

No D, C, E, c, or e antigens on cells, associated with hemolytic anemia as these structures are associated with RBC membrane integrity

Inheritance of 2 nonfunctional RHCE alleles with deletion of both RHD alleles

OR homozygous recessive inheritance of the regulator RHAG with normal RHCE and RHD

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Deleted cells (D–)

Missing some or more of the normal Rh alleles

Doesn’t react with anti-E, anti-e, anti-C, or anti-c

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Rh antibodies

Typically RBC stimulated

Pregnancy (cause hemolytic disease of the newborn as they cross the placenta)

Transfusions (will cause transfusion reactions)

IgG, do not activate complement, will not agglutinate saline suspended RBCs unless IAT is used

C/e and E/c are usually together

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Lewis Antigen Creation

Includes plasma antigens that absorb onto RBCs

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Lewis antibodies

IgM, usually only in Le(a-b-) patients, can be temporarily seen during pregnancy

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Landsteiner’s Rule

If an individual has the antigen, they will not have the antibody

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ABO Expression/makeup

Can be secreted if the proper genes are present, glycolipids or glycoproteins, develop into full expression between 2-4 years of age

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H antigen

H gene contains the alleles H and h, it is the building block for A and B antigens

Antigen is a sugar acceptor, with A and B accepting different sugars and O accepting none

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Anti-A and anti-B

IgM and therefore able to activate complement, causing agglutination

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Problems with Forward Typing

(Extra antigen, weak antigens)

ABO subgroups
Acquired B phenotype
Bone marrow/stem cell transplants
Polyagglutination
Rouleaux
Transfusion of non-specific blood

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Problems with Reverse Typing

(unexpected antibodies or weak/missing antibodies)

A subgroups with Anti-A1
Cold alloantibodies
Elderly
Newborns
Rouleaux

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Bombay Phenotype

Types as an O, with alloanti-H that can activate complement and cause hemolysis

Can transmit functional A and B genes to their children, even though they can’t produce them themselves

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Rh Genes

Controlled by RHD (D expression) and RHCE (C, c, E, e)

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Fisher-Race Terminology

Rh antigens, D, C, c, E, e, C^w, G,…

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Wiener Terminology

Rh haplotype terminology, R1, R2 for CDe/CDe

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Weak D

Weak D testing is carried out on any cell that previously gave a negative reaction with anti-D and Rh control

Caused by weaker expression of the cDe haplotype, from the C antigen is inherited trans to the D antigen

Can be transfused with D-Neg blood

Partial D

Lacking 1 or more epitopes of D antigen, and makes antibody for missing parts

Type as D Pos, create Ab after transfusion or pregnancy

F/ce antigen

Expressed when c and e are on the same haplotype

Ce/rhi antigen

Expressed when C and e are on the same haplotype, D-Pos patients who make anti-C

C^w antigen

Low frequency antigen

V/ce^s antigen

30% prevalence in African Americans

G antigen

Appears anti-D and anti-C

DAT

Use AHG (antihuman globulin) to detect IgG and complement, which indicates the possibility of immune mediated hemolysis in the patient, done for: * autoimmune hemolytic anemia * HDN (hemolytic disease of newborn) * Drug-related mechanism * Transfusion reaction

Antibody Screen

For patients needing transfusions, pregnancies, donors and those having transfusion reactions; uses O donor cells with known antigens

Hemolytic Disease of the Newborn

D- mothers makes antibodies to D+ baby in first pregnancy, newborns show positive DAT, increased serum bilirubin

2 - 5% Washed Red Cell Suspension

Visibility of antigen and antibody complexes is dependent on the number of antigen sites available

Grading Reactions with Anti-A and Anti-B

Anti-A and anti-B are saline- reactive antibodies, saline reactive antibodies are most often of the IgM class and react strongly at room temperature, and strongest at 40 C.

Antiglobulin Test

DAT * Detects in-vivo sensitization of IgG alloantibodies * IgG autoantibodies * Complement components (IAT is in-vitro)

For antiglobulin tests, why do you Incubate RBCs with antisera?

Allows time for antibody molecule attachment to RBC antigen

For antiglobulin tests, why do you Centrifuge?

Accelerates agglutination by bringing cells closer together

Albumin Reaction Media

Allows sensitized cells to come close together to form agglutination lattices

PeG Reaction Media

Concentrates Ab and creates a **low-ionic** sln that allows greater Ab uptake

ABO gene locus

C'some 9

Antigen Development

A and B develop **5th** week fetal life, but increase slowly, formed from complex interaction of H/h and ABO genes

Type 1 Precursor Chain

Glycoprotein precursor of ABH Ag

Type 2 Precursor Chain

Glycolipid precursor of ABH Ag on RBC surface

ABO Ab

* Usually IgM, can be IgG/IgA in small quantities * React best at RT * Activate complement (including the IgG at RT) * Saline agglutinins

Anti-A,B

IgG form is found in serum from sensitized O Pts (i.e. O mothers carrying A or B fetuses), which can cause HDFN

Anti-H

A weak, cold reacting Ab in A1, A1B people

Anti-A1

Non-recative a Body Temp so Clinically Insignificant, if it is reactive at that temp, it can cause in vivo RBC destruction and is clinically significant

Weak/Missing Ab

Most frequent cause of ABO discrepancy Low ABH Ab titers are found in the young, sick or debilitated and will not be picked up by routine testing, corrected by optimizing the reverse reaction conditions such as lower temp. (A/C and O cells should be controls)

Weak/Missing Ag

A/B subgroups, or weakening Ag strength in conditions like Leukemia

Acquired B Phenotype

Can be caused by intestinal obstruction, carcinoma in colon/rectum, any gastrointestinal disorder that obstructs or slows movement, allowing intestinal bacteria into bloodstream

Weak D Genetics

Caused by many different changes in the RHD gene, Types 1, 2, and 3 are 90% of the cases found in Europeans

Compound Ags

Are directed to the shared epitopes of C/c or E/e on the same protein

Immunogenicity of Rh Ag

D is most immunogenic, e is the least

Rh Testing

Use antisera that has been chemically modified with a sulflhydryl compound that weakens the disulfide bonds at the hinge region and allows the IgG to flex